INT108919
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
BACKGROUND INFORMATION: The MAPK (mitogen-activated protein kinase) superfamily of proteins consists of four separate signalling cascades: the c-Jun N-terminal kinase or stress-activated protein kinases (JNK/SAPK); the ERKs (extracellular-signal-regulated kinases); the ERK5 or big MAPK1; and the p38 MAPK group of protein kinases, all of which are highly conserved. | |||||||||||||||
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Ligand-directed c-Jun N-terminal kinase activation disrupts opioid receptor signaling. | |||||||||||||||
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Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. | |||||||||||||||
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Deletion of apoptosis signal-regulating kinase 1 attenuates acetaminophen-induced liver injury by inhibiting c-Jun N-terminal kinase activation. | |||||||||||||||
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This costimulatory signal functions through the activation of the c-Jun N-terminal kinase pathway, and it is important in lowering the threshold in response to TCR stimulation. | |||||||||||||||
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NAC inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. | |||||||||||||||
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B activation and the phosphorylation and activation of the extracellular signal-regulated kinase, Jun N-terminal kinase, and p38 mitogen-activated protein kinase pathways [56]. | |||||||||||||||
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B and Jun N-terminal kinase activation using the TNF receptor adaptor proteins TRAF1, TRAF2, and TRAF6 [36-39]. | |||||||||||||||
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activation of JNK2 in response to TPA, thereby delaying AP-1 | |||||||||||||||
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Death-promoting effects have been ascribed to inhibition of nuclear factor-kappaB, increase of Fas expression, p53 stabilization, cytokine and chemokine release, and activation of nitric oxide synthase, p38, and c-Jun-N-terminal kinase. | |||||||||||||||
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